Neuromelanin (NM) is a black pigment that accumulates in human dopaminergic and noradrenergic neurons throughout life. NM levels beyond a certain threshold are believed to be toxic contribute to neurodegeneration seen in Parkinson's disease. Here, we present a genetically encoded and cell-specific viral strategy to induce NM production in disease models, which naturally do not have detectable levels of NM. We also set out to investigate how different accumulation rates of NM in noradrenergic neurons in the locus coeruleus lead to distinct dynamics in neurodegeneration and associated changes in behavior. At a low-titer viral administration of human tyrosinase (1011 genome copies per milliliter), NM accumulated gradually in DbH-Cre mice, with observable levels first detected at 1.5 months and constantly increasing levels until the old age of 19 months (14 months post-injection), accompanied by minimal neurodegeneration. Assessments of behavior related to locus coeruleus integrity revealed no impairment, except for small changes in anxiety-like behaviors. In contrast, the administration of the virus at a higher titer (10-fold) induced rapid NM accumulation, resulting in significant locus coeruleus degeneration by 6 weeks post-injection. This was accompanied by alterations in behaviors and autonomic functions, evident as early as 3 weeks post-injection. Long-term tracking of behavior revealed accumulation-dependent changes in both individual and social behaviors. In conclusion, tyrosinase expression induced progressive NM accumulation and neurodegeneration in the locus coeruleus of mice in a viral titer dependent manner. Our experiments argue that the role of NM accumulation rate outweighs the role of its concentration in neuronal degeneration.